Gemcitabine-Induced Subacute Cutaneous Lupus Erythematosus: A Case Report

Chemotherapy ◽  
2016 ◽  
Vol 61 (5) ◽  
pp. 236-239 ◽  
Author(s):  
Masha Ben Zvi ◽  
Hananya Vaknine ◽  
Joseph Menczer ◽  
Ofri Peled ◽  
Erez Ben Shem ◽  
...  

Subacute cutaneous lupus erythematosus (SCLE) is a rare eruption related to several pharmacological and chemotherapy agents. We present a 63-year-old female with recurrent epithelial ovarian cancer who developed SCLE after administration of gemcitabine. Following discontinuation of gemcitabine and after oral steroid treatment, all skin lesions disappeared. In view of the extensive use of gemcitabine in recurrent ovarian cancer, it is important to be aware of the possibility of SCLE occurrence in these patients.

2003 ◽  
Vol 7 (3) ◽  
pp. 243-246 ◽  
Author(s):  
Emanuela Gubinelli ◽  
Barbara Cocuroccia ◽  
Giampiero Girolomoni

Background: Subacute cutaneous lupus erythematosus (SCLE) has been reported to be associated with the use of several drugs, including thiazides, terbinafine, and, rarely, calcium channel blockers. Objective: A case of SCLE induced by nifedipine is presented. Methods and Results: A 48-year-old white woman developed a papulosquamous and annular eruption in sun-exposed areas during the summer. The patient was taking nifedipine for essential hypertension for four years. Serology showed the presence of antinuclear and anti-Ro/SSA as well as antihistone antibodies. Histopathologic and immunopathologic (granular IgM deposits at the dermoepidermal junction) findings confirmed the diagnosis of SCLE. Nifedipine discontinuation led to rapid improvement with almost complete resolution of skin lesions in one month in the absence of active treatment. Reduction of antinuclear, anti-Ro/SSA, and antihistone antibody levels was documented after six months. Conclusion: Nifedipine can cause SCLE after a long period of administration. Antihistone antibodies may be associated with drug-induced SCLE.


2021 ◽  
Author(s):  
Dennis Niebel ◽  
Veronika Ralser‐Isselstein ◽  
Kristel Jaschke ◽  
Christine Braegelmann ◽  
Thomas Bieber ◽  
...  

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 217.3-217
Author(s):  
I. Calderon ◽  
R. Mina

Background:Cutaneous Lupus Erythematosus (CLE) is a disfiguring autoimmune skin disorder with several subtypes: discoid lupus, subacute cutaneous lupus, and acute cutaneous lupus. CLE is associated with defects in the adaptive immune system, and, at times, systemic involvement. The innate immune system is likely involved as seen in the presence of interface dermatitis, which is observed in viral exanthems, and improvement of CLE using inhibitors to membrane-bound Pattern Recognition Receptors.Objectives:Compare the expression of genes associated with the innate immune system in active CLE skin lesions of different subtypes compared to normal skin controls.Methods:Five datasets selected from the Gene Expression Omnibus (GEO) were analyzed using GEO2R to compare the gene expressions between different subtypes of CLE. Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database, Gene Card, and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway analysis were used to identify the interaction and function of specific genes.Results:There were a total of 147 CLE skin samples and 52 normal controls. Genes associated with the Nucleotide-Binding Oligomerization Domain-Like Receptor (NLR) signaling pathway were upregulated in CLE skin samples (adjusted p-value < 0.001). Five genes associated with the NLR signaling pathway, STAT1, OAS1, OAS2, OAS3, and AIM2, were found to be upregulated in skin samples of CLE patients in all datasets, regardless of type, compared to normal controls in all datasets. These five genes are associated with transcription activation, regulation of viral infection, and interferon response.Conclusion:Genes associated with the NLR signaling pathway are upregulated in the skin lesions of CLE patients compared to normal controls, supporting the role of the innate immune system in CLE. Further validation studies using experimental methods are needed.References:[1]Enhanced inflammasome activity in systemic lupus erythematosus is mediated via type I interferon upregulation of interferon regulatory factor 1. Liu J, et al. Arth Rheum. 2017; 69(9): 1840-1849.Disclosure of Interests:None declared


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